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Azran, L. S.

Publications and source records attributed to Azran, L. S..

2 recordsLinked to original sources

The Calcitron: A Simple Neuron Model That Implements Many Learning Rules via the Calcium Control Hypothesis

Theoretical neuroscientists and machine learning researchers have proposed a variety of learning rules for linear neuron models to enable artificial neural networks to accomplish supervised and unsupervised learning tasks. It has not been clear, however, how these theoretically-derived rules relate to biological mechanisms of plasticity that exist in the brain, or how the brain might mechanistically implement different learning rules in different contexts and brain regions. Here, we show that the calcium control hypothesis, which relates plastic synaptic changes in the brain to calcium concentration [Ca2+] in dendritic spines, can reproduce a wide variety of learning rules, including some novel rules. We propose a simple, perceptron-like neuron model that has four sources of [Ca2+]: local (following the activation of an excitatory synapse and confined to that synapse), heterosynaptic (due to activity of adjacent synapses), postsynaptic spike-dependent, and supervisor-dependent. By specifying the plasticity thresholds and amount of calcium derived from each source, it is possible to implement Hebbian and anti-Hebbian rules, one-shot learning, perceptron learning, as well as a variety of novel learning rules.

neuroscience↗

A Generalized Framework for Calcium-Based Plasticity Describes Weight-Dependent Synaptic Changes in Behavioral Time Scale Plasticity

The brain modifies synaptic strengths to store new information via long-term potentiation (LTP) and long-term depression (LTD). Evidence has mounted that long-term plasticity is controlled via concentrations of calcium ([Ca2+]) in postsynaptic spines. Several mathematical models describe this phenomenon, including those of Shouval, Bear, and Cooper (SBC) (Shouval et al., 2002, 2010) and Graupner and Brunel (GB)(Graupner & Brunel, 2012). Here we suggest a generalized version of the SBC and GB models, based on a fixed point - learning rate (FPLR) framework, where the synaptic [Ca2+] specifies a fixed point toward which the synaptic weight approaches asymptotically at a [Ca2+]-dependent rate. The FPLR framework offers a straightforward phenomenological interpretation of calcium-based plasticity: the calcium concentration tells the synaptic weight where it is going and how fast it goes there. The FPLR framework can flexibly incorporate various experimental findings, including the existence of multiple regions of [Ca2+] where no plasticity occurs, or plasticity in cerebellar Purkinje cells, where the directionality of calcium-based synaptic changes is thought to be reversed relative to cortical and hippocampal neurons. We also suggest a modeling approach that captures the dependency of late-phase plasticity stabilization on protein synthesis. We demonstrate that due to the asymptotic, saturating nature of synaptic changes in the FPLR rule, the result of frequency- and spike-timing-dependent plasticity protocols are weight-dependent. Finally, we show how the FPLR framework can explain plateau potential-induced place field formation in hippocampal CA1 neurons, also known as behavioral time scale plasticity (BTSP).

neuroscience↗